Saturday, September 6, 2025

Study Notes: Corticosteroids (Anti-inflammatory Steroids)

Study Notes: Corticosteroids (Anti-inflammatory Steroids)

I. Introduction

  • Corticosteroids = anti-inflammatory steroids.

  • Two parts of the name:

    • Steroid → hormone.

    • Cortico → related to cortisol (natural stress hormone).

  • Distinction: Not anabolic (muscle growth) steroids → these primarily reduce inflammation.

II. Cortisol & Corticosteroid Basics

  • Cortisol is made via:

    • Hypothalamus → ACTH → adrenal glands → cortisol release.

  • Negative feedback loop: High cortisol inhibits hypothalamus.

  • Receptors:

    • Glucocorticoid receptor (main therapeutic target).

    • Mineralocorticoid receptor (electrolyte balance).

III. Glucocorticoid Effects (3 main pathways)

  1. Anti-inflammatory

    • Inhibits mediators: phospholipase A₂, IL-6, TNF-α, etc.

    • ↓ Inflammation (skin, lungs, hives, etc.).

  2. Immunosuppression

    • Inhibits T-cells & B-cells → ↓ immune response.

    • Useful in transplant patients & autoimmune diseases.

  3. Metabolic (liver)

    • ↑ Glucose release (glycogen → glucose).

    • Stress response = more energy.

    • Watch for hyperglycemia in diabetics.

IV. Mineralocorticoid Effects

  • Sodium & water retention.

  • Potassium excretion.

  • Maintains fluid/electrolyte balance.

  • Clinical use: Addison’s disease, adrenal insufficiency.

V. Dosage Forms

  • Topical: Creams/ointments (hydrocortisone).

  • Oral: Prednisone, methylprednisolone (dose packs).

  • Inhaled/Intranasal: Symbicort, Flonase (asthma, allergies).

  • IV/Injectable: Dexamethasone (hospital setting).

  • Naming clue: Ends in -isone or -asone.

VI. Clinical Uses

  • Inflammation (skin irritation, tissue damage).

  • Allergic reactions (hives, anaphylaxis).

  • Asthma/COPD (inhaled steroids).

  • Autoimmune diseases (Crohn’s, MS, lupus).

  • Cancer therapy (part of regimens, premeds).

  • Adrenal insufficiency (mineralocorticoid use).

VII. Dosing & Potency

  • Hydrocortisone = baseline potency (1×).

  • Prednisone ≈ 4× stronger.

  • Methylprednisolone ≈ stronger still.

  • Dexamethasone = 25–30× stronger.

  • Relative potency + mineralocorticoid activity guide drug choice.

  • Taper required if therapy > ~6–7 days to prevent adrenal crisis.

VIII. Side Effects

  • Weight gain (reversible).

  • Fat redistribution (Cushing’s syndrome, “moon face”).

  • Edema (fluid buildup).

  • Osteoporosis (long-term use).

  • Altered mental status (mood/behavior changes).

  • Hyperglycemia (liver glucose release).

  • Hypertension.

  • Peptic ulcers.

  • Increased infection risk (immune suppression).

  • Adrenal crisis (abrupt stop → life-threatening).

IX. Quiz

  1. Well-known adverse effect of chronic systemic glucocorticoid use?
    → Osteoporosis.

  2. Common sign of iatrogenic Cushing’s syndrome?
    → Moon face (fat redistribution).

  3. Why taper after prolonged therapy?
    → Prevent adrenal crisis (due to HPA-axis suppression).

  4. Bone-related preventive measure in long-term therapy?
    → Calcium + Vitamin D supplementation, consider bisphosphonates.

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